阳和汤干预兔骨关节炎软骨细胞中血管内皮生长因子变化

目的：观察阳和汤对兔骨关节炎软骨细胞中血管内皮生长因子（vascular endothelial growth factor，VEGF）表达的影响。方法：新西兰大白兔15只随机分为正常组、模型组和阳和汤组。按照Hulth法建立膝骨关节炎模型，术后第5周起至第7周末，阳和汤组予混有阳和汤的颗粒饲料，正常组及模型组均给予普通饲料；术后第8周分别取各组胫骨平台关节软骨，采用番红O染色，进行Mankin评分；免疫组织化学染色测定关节软骨中VEGF表达的阳性指数。结果：正常对照组番红O染色的Mankin评分与模型组比较，差异有统计学意义（P〈0．01）。阳和汤组番红O染色减少或缺失程度较模型组轻，差异有统计学意义（P〈0．01）。各组关节软骨切片VEGF免疫组化染色分析，模型组VEGF的阳性指数明显高于正常组，差异有统计学意义（P〈0．01），阳和汤组VEGF阳性指数明显低于模型组，差异有统计学意义（P〈0．05）。结论：VEGF在骨关节炎形成早期起重要作用；阳和汤可延缓关节软骨退行性改变，其作用可能是通过调控VEGF而达到抑制血管增生的作用。

Effects of Yanghe Decoction on vascular endothelial growth factor in cartilage cells of osteoarthritis rabbits

OBJECTIVE: To observe the effects of Yanghe Decoction on vascular endothelial growth factor (VEGF) in cartilage cells of osteoarthritis rabbits. METHODS: Fifteen New Zealand white rabbits were randomly divided into normal group, untreated group and Yanghe Decoction-treated group. The rabbit model of osteoarthritis was established according to Hulth's method. The rabbits were sacrificed at the 8th week after administration of Yanghe Decoction for 14 days, and then rabbit tibia articular cartilage was removed. Sections of the cartilage were stained with Safranin O for histological examination. The cartilage histological characteristics were observed according to the method of Mankin. Immunohistochemical staining was performed to investigate the expression of VEGF. Articular cartilages were observed with microscopy and image analysis method was used to measure the expression intensity of VEGF. RESULTS: There were significant differences in Mankin score between normal group and untreated group (P<0.01), and between untreated group and Yanghe Decoction-treated group (P<0.01). Immunohistochemical staining indicated that the expression intensity of VEGF in untreated group was significantly increased as compared with that in normal group (P<0.01), and also obviously higher than Yanghe Decotion-treated group. CONCLUSION: VEGF plays an important role during early stage of OA. Yanghe Decoction can protect the articular cartilage through suppressing the VEGF expression in chondrocytes and then suppress angiogenesis.